Studies on the immunopathogenesis of a diversity of immune-mediated diseases and/or diseases characterized by aberrancies in immune function were performed. An intensive effort was directed at the acquired immune deficiency syndrome (AIDS). We precisely delineated the nature of the immune defect in AIDS and demonstrated that patients manifested a profound selective quantitative and qualitative defect in the T4 (Leu 3) inducer/helper subset of T lymphocytes. This has important implications in localizing the target cell of the putative infectious agent of AIDS to the T4 lymphocyte. In addition, we demonstrated a significant abnormality in B cell function in AIDS characterized by a polyclonal hyperactivity indicative of an in vivo triggering of multiple clones of B lymphocytes. We carried out a series of studies aimed at reconstitution of the defective immune function of AIDS patients. In this regard, we performed a series of lymphocyte transfers as well as a bone marrow transplant from a heterosexual well male to his homosexual identical twin brother with AIDS. Only partial reconstitution of immune function was effected and the patient continues to deteriorate suggesting that the putative agent of immunosuppression may still persist in the patient. We have also carried out studies of infusions of gamma interferon into AIDS patients in the hope of effecting at least partial reconstitution. Only equivocal results were seen. Our previous studies in which we described the first example of a primary immunodeficiency disease with an isolated defect in natural killer (NK) cells in patients with the Chediak-Higashi syndrome were extended this year. We demonstrated that patients with this syndrome have normal numbers of NK cells but have a functional defect in "active" NK cells. Finally, mechanisms of aberrant B cell activation and immunoregulation were delineated in several autoimmune diseases such as systemic lupus erythematosus and Sjogren's syndrome.